These investigations examine the biochemical pathway by which palatal fusion and steroid-induced teratogenesis is produced. The effect of the anti-inflammatory steroids on palatal teratogenesis is the depression of arachidonic acid, the precursor of prostaglandins. The way in which this produces clefting is examined through in vivo and in vitro administration of 3H-arachidonic acid and measurement of synthesis into phospholipids, prostaglandins, and triglycerides by TLC. The subcellular distribution of labelled compounds and the role of lysosomal stability in MEE autolysis is examined.